Previous work on this project has shown that value-based decision making requires both the OFC and the amygdala. We have used two kinds of tasks to investigate their mechanisms: (1) standard probabilistic and deterministic 2- and 3-choice visual discrimination learning tasks and (2) tasks that require subjects to make choices associated with rewards of different value (the devaluation task). We have found that both the amygdala and OFC are necessary when subjects need to make choices based on the current value of rewards, but not for choices based simply on the availability of rewards. Our earlier results indicated that when the value of one food was reduced by the subject consuming it to satiety, control subjects showed a reduction in actions associated with the devalued food. In contrast, subjects with either bilateral damage to the amygdala or the OFC failed to show this devaluation effect. It is well established that many animals can identify when one item is the same as another item. For example, subjects can be trained to respond to item repetitions, such as in matching paradigms, and they also naturally treat repeated objects differently than novel ones, as demonstrated in preferential viewing paradigms. It is less clear to what degree nonhuman animals possess something akin to an abstract concept of sameness that can be divorced from perceptual features. For example, we cannot only identify similarity in perceptually similar things (e.g., two dogs are the same breed), but also perceptually dissimilar things (e.g., a bullet is like an arrow), and we can conceptualize similarity as an abstract concept that can have value independent of specific objects. In the period under review we found evidence that subjects can learn a two-item same-different discrimination, and transfer this discrimination to novel stimuli. The transfer was not affected by perceptual variations in stimulus size, rotation, view, or luminance. Success on this task suggests that our subjects have a computation of sameness that is more categorical, and perhaps more abstract, than previously thought. Future studies will evaluate whether OFC and the amygdala contribute to the valuation of abstract concepts, like they do to valuation of objects and actions. We recently found that damage limited to cells in the OFC, but sparing fibers, did not affect performance on standard tests of visual discrimination learning and reversal. This led us to reject the influential idea that the primary function of the OFC involves inhibitory control. Although the loss of neurons in OFC per se is not responsible for the impairment, some other part(s) of the frontal cortex is presumably responsible. Our evidence suggests that impaired performance on reversal tasks following mechanical damage to OFC is caused by damage to white matter tracts passing nearby OFC, which disrupts the connections and functions of other frontal cortex areas. Accordingly, we set out to determine the role of both the OFC (Walkers areas 11, 13, and 14) and the ventrolateral prefrontal cortex (VLPFC, Walkers area 12), the area laterally adjacent to the OFC, in learning and reversing probabilistic stimulus-reward associations. Subjects were trained to perform a stimulus-based three-arm bandit task for food rewards. On this task, three stimuli are available for choice on each trial, and the probability of receiving a reward from any of the stimuli fluctuates over the course of 300-trial testing sessions. Both controls and subjects with lesions of the OFC were readily able to learn and track which stimulus was associated with the highest probability of reward. In contrast, subjects with lesions of VLPFC were severely impaired. Logistic regression analyses indicate that this was because subjects with VLPFC lesions were unable to form contingent associations between stimuli and rewards. Our data strongly suggest that the deficits in flexible stimulus-reward learning and reversal previously ascribed to OFC are actually the result of unintentional damage to projections to or from VLPFC. Like these recent findings for the OFC, the amygdala is not necessary for visual discrimination learning and reversal in the standard task. Indeed, amygdala damage leads to a slight facilitation in this form of stimulus-reward learning. In the period under review we developed a Bayesian approach to separately characterize two component learning processes: learning and reversing specific stimulus-reward associations and learning a higher-order rule (or belief) that reversals occur. This rule can be formally defined as a Bayesian prior belief that a reversal in the reward contingencies will occur. The object reversal learning task, therefore, requires the development of a prior belief about the probability that reversals occur. We applied the approach to behavior obtained from 89 subjects, comprising twelve lesion groups and a control group. We found that subjects from all of the groups reversed more quickly as they experienced more reversals, and correspondingly they updated their prior beliefs about reversals at the same rate. We found that across the population of subjects, reversal behavior clustered into three groups. Mechanical lesions involving OFC and rhinal cortex, as well as excitotoxic lesions of the hippocampus, lead to deficits on the task. Damage to medial OFC area 14 had no effect on task performance. Finally, selective damage to the amygdala, selective damage to OFC or parts of the medial prefrontal cortex, led to improved performance on the first few reversals. In addition, we found that the clusters differed in the initial value of their prior beliefs in reversals, but that all clusters updated their belief in reversals at the same rate. Thus, by taking a Bayesian approach we find that variability in reversal learning performance attributable to different neural systems is primarily driven by different prior beliefs about reversals that each group brings to the task. Finally, a considerable body of evidence has suggested a role for the amygdala in processing emotionally salient information in faces. To evaluate amygdala contributions to social displays of emotion, we had subjects perform an attentional capture task in which they viewed images of a socially relevant portion of a subject face (eye, nose, or mouth) or nonsocial (scrambled) images. When the image appeared at the subjects fixation point, they had to make a saccade away from it as quickly as possible. We found that both subjects with amygdala lesions and controls made saccades more slowly when they saw social vs. nonsocial images. We also found that saccade latency was significantly faster in subjects with amygdala damage, compared to controls, especially on trials with a threatening expression formed by the mouth. For comparison, we also monitored eye movements during free viewing, i.e., as subjects looked at images of faces voluntarily. In this condition, all subjects spent the greatest amount of time exploring the eye region of the face. Subjects with amygdala lesions, however, spent less time than controls exploring the eye region of the faces and more time exploring the mouth. The two tasks seem to be measuring different aspects of attention to faces. The slowing of saccades on the attentional capture task may reflect an innate response to imminent danger signals, a response that is diminished by amygdala damage. By contrast, the exploration of the eyes and mouth within a face are important to collect information about the identification and status (e.g., health, social and reproductive status) of a conspecific. Here, an influence of amygdala damage on face processing may reflect a lack of attention to social cues. These data indicate that the amygdala plays a crucial role in processing and attending to multiple aspects of face features.